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Blood, 15 October 2000, Vol. 96, No. 8, pp. 2870-2878
NEOPLASIA
Phosphorylation-deficient Stat1 inhibits retinoic acid-induced
differentiation and cell cycle arrest in U-937 monoblasts
Anna Dimberg,
Kenneth Nilsson, and
Fredrik Öberg
From the Department of Genetics and Pathology, Section
of Pathology, The Rudbeck Laboratory, Uppsala University, SE-75185,
Uppsala, Sweden.
All-trans retinoic acid (ATRA) is a potent inducer of
terminal differentiation of immature leukemic cell lines in vitro and of acute promyelocytic leukemia (APL) cells in vivo. Recent reports have shown that ATRA induces the expression of several
interferon-regulated genes, including signal transducer and activator
of transcription (Stat)1. To investigate the role of Stat1 activation
in ATRA signaling, sublines were established for the human monoblastic
cell line U-937 constitutively expressing wild-type or
phosphorylation-defective Stat1, mutated in the conserved tyrosine 701 required for dimerization and nuclear translocation. Results showed
that ATRA induction leads to activation of Stat1 by the phosphorylation
of tyrosine 701 and subsequent nuclear translocation. Consistent with a
functional importance of this activation, ectopic expression of
Stat1Y701F suppressed ATRA-induced morphologic
differentiation and expression of the monocytic surface markers CD11c
and the granulocyte colony-stimulating factor receptor. Moreover,
ATRA-induced growth arrest in the G0/G1 phase of the cell cycle was inhibited by
phosphorylation-deficient Stat1. Taken together, these results
indicate that Stat1 is a key mediator of ATRA-induced cell cycle arrest
and differentiation of U-937 cells.
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